Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030567 (Parkinson's disease)
63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We assessed the safety and efficacy of modafinil for the treatment of excessive daytime sleepiness in patients with Parkinson's disease (PD). This was a single-site, randomized, double-blind, placebo-controlled crossover study of 21 PD patients having an Epworth Sleepiness Scale (ESS) score > or =10. They received either placebo or modafinil 200 mg/day for 3 weeks, followed by a washout week, then the alternate treatment for 3 weeks. The ESS data demonstrated a carryover effect, so the changes from baseline ESS scores were compared between the two treatments for period 1 only. The ESS scores for the placebo group went from 16.0 +/- 4.2 (mean +/- SD) to 17.0 +/- 5.1 and for the modafinil group went from 17.8 +/- 4.2 to 14.4 +/- 5.7 (P = 0.039). There was no significant carryover effect for any other measure. The patient Clinical Global Impression of Change (+3 to -3) improved by 0.75 on modafinil compared with 0.15 for placebo (P = 0.07). A total of 7 of 20 (35%) of the patients reported some improvement on modafinil but not placebo. There was no significant improvement or worsening of the UPDRS subscores I-III, Timed Tap test, or time on. Vital signs, electrocardiograms, and lab tests were unchanged. Modafinil was very well tolerated. Our data demonstrate that, in a small sample size, administration of 200 mg/day of modafinil was associated with few side effects and was modestly effective for the treatment of excessive daytime sleepiness in patients with PD.
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PMID:Randomized trial of modafinil for treating subjective daytime sleepiness in patients with Parkinson's disease. 1262 32

We evaluated the frequency and severity of excessive daytime sleepiness in an outpatient population with Parkinson's disease in comparison to age-matched controls and examined its relationship with antiparkinsonian drug therapy and sleep history. Increased daytime sleepiness and involuntary sleep episodes have been described in Parkinson's disease, but the etiology is not completely understood. The Epworth Sleepiness Scale (ESS), a validated questionnaire for daytime sleepiness, was prospectively administered to 99 consecutive outpatients with Parkinson's disease and 44 age-matched controls. In addition, a short sleep-screening questionnaire was used. The ESS revealed significantly increased daytime sleepiness in PD patients compared to controls (7.5 +/- 4.6 vs. 5.8 +/- 3.0, P = 0.013). The ESS score was abnormally high (10 or more) in 33 % of PD patients and 11.4% of controls (P = 0.001). ESS was not different between PD patients on levodopa monotherapy and those on levodopa and dopamine agonists, or between patients taking ergoline or non-ergoline dopamine agonists. In PD patients and in controls, sleepiness was significantly associated with reported heavy snoring. Increased daytime sleepiness is more frequent in patients with PD than in elderly controls. Similar to controls, increased daytime sleepiness in PD patients is correlated with heavy snoring.
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PMID:Increased daytime sleepiness in Parkinson's disease: a questionnaire survey. 1262 36

Sleep disorders are common in Parkinson's disease (PD), as almost two thirds of PD patients report them. From a clinical point of view, they can be classified into disorders of initiation and maintenance of sleep (DIMS), parasomnias, and excessive daytime sleepiness (EDS). Among the causes of DIMS are degenerative changes in the CNS affecting centers for sleep regulation, persistence into the night of daytime PD-related symptoms, concomitant medical or psychiatric disease, disruption of circadian rhythms, and effects of dopaminergic (and other) medication on sleep regulation. Parasomnias might further contribute to sleep disturbance, as they can be accompanied by motor desinhibition during REM sleep. Parasomnias can precede by several years the presence of daytime PD symptoms. EDS has been over the last years the focus of attention for both sleep and movement disorders specialists, due to the fact that it might predispose to traffic accidents. However, the so-called "sleep attacks" never occur without preexisting somnolence. Thus, a careful sleep history can be helpful to determine which patients are exposed to suffer them. Although EDS was initially attributed to the effects of dopaminergic medication, it seems likely that several disease-related factors might also play an important role. An adequate education of the PD patients in sleep hygiene measures and a skilled use of the medication seem necessary to prevent sleep disturbance.
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PMID:Parkinson's disease and sleep. 1262 13

Patients with Parkinson's disease (PD) and parkinsonian syndromes (eg, dementia with Lewy bodies, multisystem atrophy, and Shy-Drager syndrome) suffer from daytime sleepiness. Sleepiness in PD is common (10% to 50% of patients) and very real, often approaching levels observed in the prototypical disorder of sudden-onset sleep, viz, and narcolepsy with cataplexy. Physicians need to be vigilant in assessing parkinsonian patients for sleepiness, because treatment can dramatically enhance quality of life and prevent the significant morbidity and mortality that attends daytime sleepiness. Men with advanced disease, cognitive impairment, drug-induced psychosis, and orthostatic hypotension are most at risk for developing pathologic sleepiness. Because primary sleep disorders can coexist with Parkinsonism (eg, sleep apnea, insufficient or interrupted sleep), these potential causes should be carefully assessed with polysomnography and treated appropriately. Dopaminomimetics may exacerbate sleepiness in a small subset of patients. The primary pathologies involved in Parkinsonism appear to be the greatest contributors to the development of daytime sleepiness. Sleepiness in Parkinsonism, especially a narcolepsy-like phenotype, may necessitate treatment with wake-promoting agents, such as bupropion, modafinil, or traditional psychostimulants.
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PMID:Sleepiness and Unintended Sleep in Parkinson's Disease. 1267 Apr 12

Hallucinations (mainly visual), psychosis and excessive daytime sleepiness are potential side-effects of dopaminergic treatment. They may require a reduction or suppression of dopaminergic agonists, and the prescription of atypical neuroleptic agents or vigilance-enhancing drugs. The recent description of narcolepsy-like sleep onset in rapid eye movement sleep periods synchronous with hypnagogic hallucinations in patients with dopaminergic-induced psychosis or excessive daytime sleepiness, suggests that the mesodiencephalic lesions may predispose to the psychic effects of dopaminergic treatment. Disease-related mood disorders, sexual compulsions, gambling or levodopa addiction may also be amplified by the antiparkinsonian treatment. These complications illustrate the neuro-psychic aspect of Parkinson's disease: psychic troubles may result from a subtle balance between the direct effects of drugs, the pre-morbid pathological personality and the cortical and subcortical lesions.
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PMID:[Psychic disorders and excessive daytime sleepiness] 1269 Mar 20

Hallucinations (mainly visual), psychosis and excessive daytime sleepiness are potential side-effects of dopaminergic treatment. They may require a reduction or suppression of dopaminergic agonists, and the prescription of atypical neuroleptic agents or vigilance-enhancing drugs. The recent description of narcolepsy-like sleep onset in rapid eye movement sleep periods synchronous with hypnagogic hallucinations in patients with dopaminergic-induced psychosis or excessive daytime sleepiness, suggests that the mesodiencephalic lesions may predispose to the psychic effects of dopaminergic treatment. Disease-related mood disorders, sexual compulsions, gambling or levodopa addiction may also be amplified by the antiparkinsonian treatment. These complications illustrate the neuro-psychic aspect of Parkinson's disease: psychic troubles may result from a subtle balance between the direct effects of drugs, the pre-morbid pathological personality and the cortical and subcortical lesions.
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PMID:[Psychic disorders and somnolence]. 1269 Jun 69

In recent years, sleep abnormalities have increasingly been observed in patients with movement disorders. During sleep, most patients with Parkinson's disease also exhibit the movements characteristically seen during the wake period. Movement activity during sleep may impair sleep quality and lead to daytime sleepiness and reduced quality of life. Disordered REM sleep with enhanced muscle tone is common in patients with neurodegenerative disease, and may precede the clinically evident symptoms of Parkinson's disease by years. Sleep disorders in patients with Parkinson's disease are common, and require the application of individual treatment strategies. A further frequent disorder primarily classified as a sleep disorder (dyssomnia) is the restless legs syndrome (RLS), which is closely related to the nocturnal periodic limb movement disorder and affects up to 15% of the population. The present review focuses on nocturnal motor activity and sleep in Parkinson's disease and RLS.
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PMID:Movement disorders in sleep: Parkinson's disease and restless legs syndrome. 1270 36

We sought to determine whether mirtazapine is safe and well-tolerated as a treatment for essential tremor (ET). We studied mirtazapine in a randomized, double-blind, placebo-controlled, crossover study of 17 ET patients. Patients were started with 15 mg per day of either mirtazapine or placebo for 1 week and the dose was escalated weekly until the targeted dose of 45 mg per day was achieved. This dose was maintained for 2 weeks. Tremor was assessed at baseline and after 14 days of 45 mg of mirtazapine or placebo. There was a minimum washout period of 14 days between the two arms of the study. Tremor assessments included global improvement, Fahn Tolosa Marin Tremor Rating Scale, Beck Depression Inventory and the Parkinson's Disease Questionnaire-39. Patient global improvement ratings indicated that in the placebo condition 12 patients were unchanged and 1 patient was mildly improved. In the mirtazapine condition, 10 patients were unchanged, 2 were moderately improved and 1 was markedly improved. There was no significant improvement with mirtazapine or placebo compared to baseline as measured by the Tremor Rating Scale. Adverse effects were more common in the mirtazapine group and included drowsiness, confusion, dry mouth, weight gain, polyuria, itching, nausea, gait and balance problems, blurred vision, and bad taste. We conclude that the majority of the ET patients do not benefit from mirtazapine. Mirtazapine has significant adverse effects and should be used cautiously in ET patients.
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PMID:Mirtazapine in essential tremor: a double-blind, placebo-controlled pilot study. 1272 74

The aetiology of sleep disturbances in patients with Parkinson's disease is multifactorial. Medications, the disease process and underlying sleep disorders may contribute to sleepiness in patients with the disease. Somnolence, excessive daytime sleepiness and sleep attacks appear to be more common in patients with Parkinson's disease who are treated with dopamine receptor agonists than in those who are treated with other antiparkinsonian agents, although virtually all dopaminergic antiparkinsonian medications may contribute to sleepiness. Somnolence caused by dopamine agonists may be dose related and occurs most frequently during the dose-escalation phase. Somnolence may also emerge or worsen after a period of time on a stable dose. Patients with Parkinson's disease and caregivers should be informed about the risk of sleepiness and sleep attacks associated with dopaminergic medications and the potential implications for driving safety.
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PMID:Sleep attacks and dopamine agonists for Parkinson's disease: what is currently known? 1277 95

Parkinson's disease (PD) is a progressive neurodegenerative disease that is caused by a loss of neurons in the ventral midbrain. Parkinsonian patients often experience insomnia, parasomnias, and daytime somnolence. REM sleep behavior disorder (RBD) is characterized by vigorous movements during REM sleep, and may also be caused by neuronal degeneration in the central nervous system (CNS); however, the site of degeneration remains unclear. Both Parkinsonism and RBD become more prevalent with aging, with onset usually occurring in the sixties. Recent findings show that many individuals with RBD eventually develop Parkinsonism. Conversely, it is also true that certain patients diagnosed with Parkinsonism subsequently develop RBD. Postmortem examination reveals that Lewy bodies, Lewy neurites, and alpha-synuclein are found in brainstem nuclei in both Parkinsonism and RBD patients. In this article, we will discuss evidence that Parkinsonism and RBD are physiologically and anatomically linked, based on our animal experiments and other studies on human patients.
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PMID:Physiological and anatomical link between Parkinson-like disease and REM sleep behavior disorder. 1277 84


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